Iron deficient and anemic humans and rats fail to maintain body temperature when cold stressed. It is not clear from existing data how much of this thermoregulatory defect is secondary to the anemic associated with iron deficiency. Exchange transfusion acutely improves body temperature maintenance, (TSH) response, thyroxine (T4) response and triiodothyronine (T3) response of iron deficient animals to a cold stress. Elevated plasma and urine norepinephrine (NE) levels are unaffected by this correction of anemia. Accurate data on metabolic rate, tissue NE turnover, thyroid hormone metabolism or actual thermogenic activity relative to the anemia are lacking. The major goal of this proposal is to define the relationships of catecholamine metabolism to decreased thermoregulatory capacity in iron deficiency anemia. The major hypothesis being tested is that increased SNS activity in iron deficiency is compensatory to perhaps impaired thyroid hormone function (model adapted from Cannon). Several key concepts need to be established as intermediate goals before the underlying effects of iron deficiency anemia on thermogenesis are examined. First: Are the minimum metabolic, and the maximal NE stimulated metabolic rates different in ID and control rats and affected by anemia? Second: What is the resting metabolic rate relationship to temperature in ID compared to controls? Third: Is sympathetic nervous system activity increased in ID at low temperatures? The underlying processes whereby the anemia of iron deficiency may affect thermogenesis are examined by quantification of blood flow (microspheres) to thermogenic organs, rates of conversion of thyroxine to triiodothyronine (liver and brown adipose tissue (5I-deiodinase), BAT thermogenic activity (NE turnover and mito. GDP binding). The accurate documentation of metabolic rate and SNS activity in IDA will provide a good base for understanding the thermoregulatory defects. Future studies may then examine possible effects of tissue iron deficiency on hormone conversion, receptor site regulation, mitochondrial dysfunction, and/or abnormal CNS control of thermogenesis.